Glucagon-Induced Growth Hormone Release in Children

Weber, Bruno; Helge, H; Quabbe, Hans-Jürgen

doi:10.1530/acta.0.0650323

Cited by 26 publications

(5 citation statements)

References 15 publications

(18 reference statements)

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“…were recorded [28,74,76], which led to discontinuation of the test in one study in 2/13 children [28]. In the case of clonidine testing, a transient decrease in blood pressure and drowsiness was recorded [25,49,71].…”

mentioning

confidence: 99%

Impact of body mass index on growth hormone stimulation tests in children and adolescents: a systematic review and meta-analysis

Abawi

Augustijn

Hoeks

et al. 2021

Critical Reviews in Clinical Laboratory Sciences

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mentioning

confidence: 99%

Impact of body mass index on growth hormone stimulation tests in children and adolescents: a systematic review and meta-analysis

Abawi

Augustijn

Hoeks

et al. 2021

Critical Reviews in Clinical Laboratory Sciences

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“…In humans, aberrant expression of glucagon can be associated with pathophysiological or disease conditions (e.g., diabetes, non-alcoholic fatty liver, and glucagon-producing tumor) (5). In mammals, positive correlation between circulating levels of glucagon and growth hormone (GH) (6) and glucagon-induced GH secretion are well-documented (7, 8), suggesting a functional crosstalk of the somatotropic axis with glucagon. However, the effect of glucagon on hepatic expression of IGF-I, the downstream effector for GH, is controversial, as both stimulatory (9) and inhibitory effects (10) have been reported (e.g., in rat hepatocytes).…”

Section: Introductionmentioning

confidence: 99%

Novel Mechanisms for IGF-I Regulation by Glucagon in Carp Hepatocytes: Up-Regulation of HNF1α and CREB Expression via Signaling Crosstalk for IGF-I Gene Transcription

Bai

Jiang

et al. 2019

Front. Endocrinol.

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Glucagon, a key hormone for glucose homeostasis, can exert functional crosstalk with somatotropic axis via modification of IGF-I expression. However, its effect on IGF-I regulation is highly variable in different studies and the mechanisms involved are largely unknown. Using grass carp as a model, the signal transduction and transcriptional mechanisms for IGF-I regulation by glucagon were examined in Cyprinid species. As a first step, the carp HNF1α, a liver-enriched transcription factor, was cloned and confirmed to be a single-copy gene expressed in the liver. In grass carp hepatocytes, glucagon treatment could elevate IGF-I, HNF1α, and CREB mRNA levels, induce CREB phosphorylation, and up-regulate HNF1α and CREB protein expression. The effects on IGF-I, HNF1α, and CREB gene expression were mediated by cAMP/PKA and PLC/IP3/PKC pathways with differential coupling with the MAPK and PI3K/Akt cascades. During the process, protein:protein interaction between HNF1α and CREB and recruitment of RNA Pol-II to IGF-I promoter also occurred with a rise in IGF-I primary transcript level. In parallel study to examine grass carp IGF-I promoter activity expressed in αT3 cells, similar pathways for post-receptor signaling were also confirmed in glucagon-induced IGF-I promoter activation and the trans-activating effect by glucagon was mediated by the binding sites for HNF1α and CREB located in the proximal region of IGF-I promoter. Our findings, as a whole, shed light on a previously undescribed mechanism for glucagon-induced IGF-I gene expression by increasing HNF1α and CREB production via functional crosstalk of post-receptor signaling. Probably, by protein:protein interaction between the two transcription factors and subsequent transactivation via their respective cis-acting elements in the IGF-I promoter, IGF-I gene transcription can be initiated by glucagon at the hepatic level.

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“…Moreover, the HPA response to i.m. glucagon is unlikely to be related to glucose variations and stress-mediated actions (1,4,10,11,14). Moreover, glucagon does not act at the pituitary level (10).…”

Section: Introductionmentioning

confidence: 99%

“…On the other hand, a role of glucagon-induced free fatty acids (13), but not glycemic (1,4,10,11,14) variations have also been suggested.…”

Section: Introductionmentioning

confidence: 99%

Interaction between glucagon and human corticotropin-releasing hormone or vasopressin on ACTH and cortisol secretion in humans

Arvat

Maccagno

Ramunni

et al. 2000

European Journal of Endocrinology

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Objective: It is known that glucagon administration elicits ACTH and cortisol responses in humans, although this effect takes place after intramuscular or subcutaneous but not after the intravenous route of administration. The mechanisms underlying this stimulatory effect on corticotroph secretion are unknown but they are unrelated to glucose variations and stress-mediated actions. Design and Methods: To throw further light on the stimulatory effect of i.m. glucagon on the pituitary± adrenal axis, using six normal young female volunteers (26±32 years, body mass index 19.7±22.5 kg/m 2 ) we studied the interaction between glucagon (GLU; 0.017 mg/kg i.m.) and human corticotropinreleasing hormone (hCRH; 2.0 mg/kg i.v.) or vasopressin (AVP; 0.17 U/kg i.m.). The interactions between hCRH and AVP on the hypothalamo±pituitary±adrenal (HPA) axis and the GH response to GLU alone or combined with hCRH or AVP were also studied. Results: GLU i.m. administration elicited a clear increase in ACTH (peak vs baseline, means 6 S.E.M.: 11.6 6 3.3 vs 4.2 6 0.3 pmol/l, P < 0.05), cortisol (613.5 6 65.6 vs 436.9 6 19.3 nmol/l, P < 0.05) and GH levels (11.6 6 3.4 vs 3.3 6 0.7 mg/l, P < 0.05). The ACTH response to GLU (area under the curve: 426.4 6 80.9 pmol/l per 120 min) was higher than that to AVP (206.3 6 38.8 pmol/l per 120 min, P < 0.02) and that to hCRH (299.8 6 39.8 pmol/l per 120 min) although this latter difference did not attain statistical signi®cance. The GLU-induced cortisol response (28 336.9 6 2430.7 nmol/l per 120 min) was similar to those after hCRH (24 099.2 6 2075.2 nmol/l per 120 min) and AVP (21 808.7 6 1948.2 nmol/l per 120 min). GLU and hCRH had an additive effect on ACTH (964.9 6 106.6 pmol/l per 120 min, P < 0.02) and a less than additive effect on cortisol levels (35 542.5 6 2720.2 nmol/l per 120 min). Similarly, GLU and AVP had an additive effect on ACTH (825.6 6 139.6 pmol/l per 120 min, P < 0.02) and an effect less than additive on cortisol levels (33 059.2 6 1965.3 nmol/l per 120 min). The effects of GLU co-administered with hCRH or AVP were similar to those of the combined administration of hCRH and AVP on ACTH (906.0 6 152.7 pmol/l per 120 min) and cortisol (34 383.5 6 1669.2 nmol/l per 120 min) levels. The GH response to GLU was not modi®ed by hCRH or AVP. Conclusions: These results show that i.m. glucagon administration is a provocative stimulus of ACTH and cortisol secretion, at least as potent as hCRH and AVP. The ACTH-releasing effect of i.m. glucagon is not mediated by selective CRH or AVP stimulation but the possibility that both neurohormones play a role could be hypothesized. European Journal of Endocrinology 143 99±104

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Glucagon-Induced Growth Hormone Release in Children

Cited by 26 publications

References 15 publications

Impact of body mass index on growth hormone stimulation tests in children and adolescents: a systematic review and meta-analysis

Impact of body mass index on growth hormone stimulation tests in children and adolescents: a systematic review and meta-analysis

Novel Mechanisms for IGF-I Regulation by Glucagon in Carp Hepatocytes: Up-Regulation of HNF1α and CREB Expression via Signaling Crosstalk for IGF-I Gene Transcription

Interaction between glucagon and human corticotropin-releasing hormone or vasopressin on ACTH and cortisol secretion in humans

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